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Mitochondrial Integrity and Function in the Progression of Early Pressure Overload-Induced Left Ventricular Remodeling. | LitMetric

AI Article Synopsis

  • The study investigates how compensatory concentric left ventricular remodeling (CR) transitions to eccentric remodeling (ER) and systolic dysfunction following pressure overload in rats.
  • Researchers found that different phenotypes of remodeling emerged after aortic banding, showing variations in heart function and characteristics despite similar pressure overload.
  • Key observations included increased mitochondrial biogenesis and normal calcium handling in CR and mild ER, while moderate ER exhibited impaired mitochondrial function and increased signs of cell death, occurring before the development of significant systolic dysfunction.

Article Abstract

Background: Following pressure overload, compensatory concentric left ventricular remodeling (CR) variably transitions to eccentric remodeling (ER) and systolic dysfunction. Mechanisms responsible for this transition are incompletely understood. Here we leverage phenotypic variability in pressure overload-induced cardiac remodeling to test the hypothesis that altered mitochondrial homeostasis and calcium handling occur early in the transition from CR to ER, before overt systolic dysfunction.

Methods And Results: Sprague Dawley rats were subjected to ascending aortic banding, (n=68) or sham procedure (n=5). At 3 weeks post-ascending aortic banding, all rats showed CR (left ventricular volumes < sham). At 8 weeks post-ascending aortic banding, ejection fraction was increased or preserved but 3 geometric phenotypes were evident despite similar pressure overload severity: persistent CR, mild ER, and moderate ER with left ventricular volumes lower than, similar to, and higher than sham, respectively. Relative to sham, CR and mild ER phenotypes displayed increased phospholamban, S16 phosphorylation, reduced sodium-calcium exchanger expression, and increased mitochondrial biogenesis/content and normal oxidative capacity, whereas moderate ER phenotype displayed decreased p-phospholamban, S16, increased sodium-calcium exchanger expression, similar degree of mitochondrial biogenesis/content, and impaired oxidative capacity with unique activation of mitochondrial autophagy and apoptosis markers (BNIP3 and Bax/Bcl-2).

Conclusions: After pressure overload, mitochondrial biogenesis and function and calcium handling are enhanced in compensatory CR. The transition to mild ER is associated with decrease in mitochondrial biogenesis and content; however, the progression to moderate ER is associated with enhanced mitochondrial autophagy/apoptosis and impaired mitochondrial function and calcium handling, which precede the onset of overt systolic dysfunction.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5669187PMC
http://dx.doi.org/10.1161/JAHA.117.005869DOI Listing

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